Arrhythmias are abnormal heart rhythms that may cause the heart to function less effectively. Atrial fibrillation (AF) is the most common abnormal heart rhythm. In AF, the two upper chambers of the heart (i.e., the atria) quiver rather than beat and, consequently, fail to entirely empty of blood. As blood stagnates on the walls of the atria, it may form thrombi (i.e., clots). Under certain circumstances, these thrombi can re-enter circulation and travel to the brain, causing a stroke or a transient ischemic attack (TIA).
Research has indicated that as many as ninety (90) percent of all thrombi formed during AF originate in the left atrial appendage (LAA). The LAA 11 is a remnant of an original embryonic left atrium that develops during the third week of gestation. As shown in FIG. 1, it is located high on the free wall of the left atrium 12. Long, tubular, and hook-like in structure, the LAA 11 is connected to the left atrium 12 by a narrow junction 14, referred to as the “ostium” (FIG. 1). The precise physiological function of the LAA remains uncertain. Recent reports suggest it may maintain and regulate pressure and volume in the left atrium; modulate the hemodynamic response during states of cardiac stress; mediate thirst in hypovolemia; and/or serve as the site of release of both the peptide hormone atrial natriuretic factor (ANF), which stimulates excretion of sodium and water by the kidneys and regulates blood pressure, and stretch sensitive receptors, which regulate heart rate, diuresis, and natriuresis.
The high rate of thrombus formation in the LAA is believed to be attributable to its physical characteristics. Blood easily stagnates and thereafter can clot in the long, tubular body of the LAA or at its narrow ostium. In contrast, a right atrial appendage (RAA), which is a wide, triangular appendage connected to the right atrium by a broad ostium, is infrequently the site of thrombus formation. Thrombus formation in the LAA is further promoted by the numerous tissue folds 13 (i.e., crenellations) on its interior surface (FIG. 1). These crenellations 13 are particularly hospitable to blood stagnation and clotting, especially when the heart is not functioning at maximum capacity. Thrombi formed in the LAA can re-enter the circulation upon conversion of AF to normal rhythm (i.e., cardioversion).
Certain patient subsets are considered to be at an abnormally high risk of thrombus formation. Such patients include those over seventy-five (75) years of age, as well as those presenting with a history of thromboembolism, significant heart diseases, decreased LAA flow velocity, increased LAA size, spontaneous echogenic contrast, abnormal coagulation, diabetes mellitus, and/or systemic hypertension. For these high-risk patients, prophylactic intervention may be recommended. Currently proposed prophylaxes generally fall into three categories: (1) surgical ligation of the LAA; (2) implantation of an LAA occluder sufficient to prevent, or at least minimize, blood flow into the LAA; and (3) placement of a filter in the LAA ostium to prevent clots formed therein from re-entering the circulatory system.
Because of the uncertain physiological role of the LAA, its obliteration and occlusion are controversial. Reports have suggested that obliteration of the LAA may decrease atrial compliance and diminish ANF secretion. Furthermore, while properly positioned filter devices prevent migration of thrombi into the circulatory system, they cannot inhibit thrombus formation within the LAA. Consequently, in the event the filter device is dislodged or ineffectively sealed against the LAA ostium, clots held at the LAA ostium by the filter could be released into the circulation.